Ebolahemorrhagic fever (EHF) is an acute infectious disease caused by the Ebola virus (Ebolavirus, EBV), which was first identified in Africa in the 1970s. It has been endemic in central Africa since 1976, when outbreaks occurred in Zaire (now the Democratic Republic of Congo) and Sudan. The clinical manifestations are mainly fever, hemorrhage and multiple organ damage. Ebola hemorrhagic fever has a high morbidity and mortality rate, and seriously endangers the health of the population in the infected area. I. Pathogenesis Ebola virus belongs to filovirus family, including four subtypes: Ebola-Zaire (Ebola-Zare), Ebola-Sudan (Ebola-Sudan), Ebola-Côte d’Ivoire (Ebola-Cted’Ivoire) and Ebola-Reston (Ebola-Reston). Three subtypes of Ebola occurring in Congo (formerly Zaire), Sudan, and Côte d’Ivoire have been shown to cause human disease. The virulence of the different subtypes varies, with Ebola-Zare being highly virulent with high human mortality, Ebola-Sudan being second, Ebola-Cted’Ivoire being lethal in chimpanzees and less virulent in humans, and Ebola-Reston being lethal in non-human primates with no human morbidity. EBV has various morphologies, rod-shaped, filamentous, and “L” shaped, with an average particle length of 1000 nm and a diameter of 70-90 nm. The EBV genome is an unsegmented negative-stranded RNA, 18.9 kb in size, encoding 7 structural proteins and 1 non-structural protein. EBV virus is mostly inactivated at 60°C for 1 h. UV, γ-rays, formaldehyde, hypochlorous acid, phenolic disinfectants and lipid solvents can inactivate the virus. EBV proliferates in human, monkey, guinea pig and other mammalian cells, with Vero-98, Vero-E6 and Hela-229 cells being the most sensitive. The cytopathic lesions appear 6-7 hours after virus inoculation and are characterized by rounding and crinkling of cells, and inclusion bodies with fibrous or granular structures are seen in the cytoplasm. Epidemiology Ebola hemorrhagic fever is mainly prevalent in Uganda, Congo, Gabon, Sudan, Cote d’Ivoire, Liberia, South Africa and other countries in Africa. (A) Infectious source and host. Both human and non-human primates infected with Ebola virus can be the infectious source of the disease. On the African continent, Ebola virus infection has been associated with contact with wild animals such as chimpanzees, gorillas, and monkeys that died in the rainforest. IgG antibodies to Ebola virus have been detected in the sera of three species of African fruit bats, and Ebola virus nucleic acids have been detected in the liver and spleen. There is experimental confirmation that bats do not die after infection with Bola virus. Bats may play an important role in maintaining the presence of Ebola virus in tropical forests. (ii) Transmission routes. 1. Contact transmission: Contact transmission is the most important route of transmission of the disease, which is spread by contact (especially blood, excreta and other contaminants) between patients and subclinically infected persons with the virus. Intra-hospital transmission is an important factor leading to outbreak epidemics of Bola hemorrhagic fever. (2) Aerosol transmission: inhalation of infectious secretions, excretions, etc. (iii) Population susceptibility. Humans are generally susceptible to Ebola virus. After the virus enters the body, it may first infect monocytes, macrophages and other cells of the mononuclear phagocytic system (mononuclearphagocyticsystem, MPS) in local lymph nodes. Some infected MPS cells metastasize to other tissues, and when the virus is released into the lymph or blood, it can cause infection of the liver, spleen, and fixed or mobile macrophages throughout the body. Viruses released from MPS cells can infect adjacent cells, including hepatocytes, adrenal epithelial cells, and fibroblasts. Infected MPS cells are simultaneously activated and release large amounts of cytokines and chemokines, including tumor necrosis factor (TNF). These cytoactive substances increase the permeability of vascular endothelial cells, induce the expression of endothelial cell surface adhesion and procoagulant factors, as well as the exposure of collagen in the vessel wall after tissue destruction and the release of tissue factor, ultimately leading to disseminated intravascular coagulation (DIC). Massive apoptosis of lymphocytes in the spleen, thymus and lymph nodes may occur in the late stage of infection. The main pathological changes are hemorrhage of the skin, mucous membranes, and organs, and focal necrosis can be seen in many organs, but is most severe in the liver and lymphoid tissue. Punctate and focal necrosis of hepatocytes is the most striking feature of the disease, and small inclusion bodies and apoptotic vesicles are seen.